Why the study?
How does the mode of delivery (vaginal vs abdominal) affect maternal urinary 6-keto-PGF1 alpha excretion?
How does the mode of delivery (vaginal vs abdominal) affect maternal urinary 6-keto-PGF1 alpha excretion?
Both vaginal and abdominal delivery are accompanied by significant increases in maternal prostacyclin release, which may help regulate fetoplacental blood flow and prevent peripartum thrombosis.
Greater prostacyclin release after caesarean may reflect surgical stress; leaves open differential effects on peripartum thrombosis risk.
To study the role of the antiaggregatory and vasodilatory prostacyclin (PGI2) during human delivery, serial urine samples collected from 13 women delivered vaginally and from eight delivered abdominally were assayed for 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha, a breakdown product of PGI2) by high-performance-liquid-chromatography and radioimmunoassay. In women delivered vaginally the mean urinary 6-keto-PGF1 alpha concentration was 41.9 (SE 8.3) ng/mmol creatinine, before the onset of labour and increased progressively to a maximum of 186.5 (SE 47.6) ng/mmol creatinine 2 h after delivery irrespective of the use of oxytocin and epidural analgesia. In women delivered by caesarean section under epidural anaesthesia, the urinary 6-keto-PGF1 alpha rose from 33.4 (SE 4.2) ng/mmol creatinine to 2153 (SE 314) ng/mmol creatinine 2 h after section. In both groups the increased levels had fallen by 24 h postpartum to levels below those found before delivery. In neonatal urine 6-keto-PGF1 alpha concentrations were some 12-30 times higher than those in postpartum urine. Thus, vaginal and abdominal delivery is accompanied by significant increases in maternal PGI2 release, perhaps in the myometrium and/or intrauterine tissues. This may be of significance in the regulation of fetoplacental blood flow and in the prevention of intra- and postpartum thrombosis.
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Ylikorkala et al. (1986) studied this question.
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